title: Underlying pathways for interferon risk to type II diabetes mellitus.
abstract: It has been known that chronic liver treatments interfere with blood glucose metabolism. It was recognized that diabetes mellitus among chronic hepatitis C was greater in other types of chronic liver diseases. Hepatitis C directly promotes insulin resistance through the proteosomal degradation of insulin resistance substrate. It suppressed hepatocyte glucose uptake through down-regulation of surface expression of glucose transporter. Long-term exposure to cytokine over expression seems to be cytotoxic to both beta cells of the pancreas and to hepatocytes. Elevated tumor necrosis factor-a, or its neutralization, increased insulin sensitivity. Interferon-a may also elevate the serum level of interleukin-1 which is cytotoxic to pancreatic islet cells. Both diabetes mellitus and resistance to interferon-a therapy are abnormally mediated by over-expression of suppressor of cytokine signaling-1 in hepatocytes of chronic hepatitis C patients.
  
  
  CONCLUSIONS
  These data suggest that interferon-a therapy should be administered with caution in patients showing any predisposition to Diabetes mellitus. Anti inflammatory therapy is critically recommended as a protector against disease development due to cytokine mediated Diabetes mellitus during hepatitis C therapy, since inflammation seems to be a main candidate to interferon suspected diabetogenesis.
authors.affiliation: Dean of College of Pharmacy, Kafrelsheikh University, Egypt. taghreidkheder@yahoo.com.
authors.forename: Nabil
authors.initials: N
authors.lastname: Abdel-Hamid
authors.forename: Taghreed Al
authors.initials: TA
authors.lastname: Jubori
authors.forename: Amaal
authors.initials: A
authors.lastname: Farhan
authors.forename: Mariam
authors.initials: M
authors.lastname: Mahrous
authors.forename: Adel
authors.initials: A
authors.lastname: Gouri
authors.forename: Ezzat
authors.initials: E
authors.lastname: Awad
authors.forename: Johannes
authors.initials: J
authors.lastname: Breuss
mesh_terms: D000998:Antiviral Agents / Q000008:administration & dosage / Q000009:adverse effects*; D001786:Blood Glucose / Q000378:metabolism; D003924:Diabetes Mellitus, Type 2 / Q000139:chemically induced / Q000276:immunology* / Q000503:physiopathology; D015536:Down-Regulation; D005260:Female; D019698:Hepatitis C, Chronic / Q000188:drug therapy / Q000276:immunology* / Q000503:physiopathology; D006801:Humans; D007249:Inflammation / Q000139:chemically induced / Q000276:immunology* / Q000503:physiopathology; D007333:Insulin Resistance; D016898:Interferon-alpha / Q000008:administration & dosage / Q000009:adverse effects*; D007375:Interleukin-1 / Q000097:blood / Q000378:metabolism; D008297:Male; D018579:Patient Selection; D015398:Signal Transduction; D050826:Suppressor of Cytokine Signaling Proteins / Q000096:biosynthesis / Q000187:drug effects; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D000998:Antiviral Agents; D001786:Blood Glucose; D016898:Interferon-alpha; D007375:Interleukin-1; D050826:Suppressor of Cytokine Signaling Proteins; D014409:Tumor Necrosis Factor-alpha